High concentrations of caffeine significantly alter electrophysiological properties of rat ventricular myocytes, including lengthening action potential duration and depressing key inward currents, which must be accounted for in electromechanical coupling studies.
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Caffeine effects on APD and currents require controls in rat myocyte studies; leaves open translation to in vivo or human models.
The effects of high (20 mM) concentrations of caffeine were studied on the transmembrane voltage and currents in rat single ventricular myocytes by the whole cell configuration of the patch clamp technique. Rapid application of caffeine released Ca2+ from the sarcoplasmic reticulum and induced a Ni(2+)-sensitive transient inward current with concomitant change of the transmembrane voltage from -72.6 +/- 0.4 to -68.0 +/- 0.6 mV (n = 4). Maintained application of caffeine lengthened the action potential duration (APD90) from 66.7 +/- 16.9 to 135.1 +/- 34.1 ms (n = 4) and depressed the amplitude of both the inward rectifier potassium and the inward calcium currents. It is concluded that these effects of caffeine should be recognized when it is used as a tool to study electromechanical coupling.
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Varró et al. (1993) studied this question.
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